Preferential attack of mitochondrial DNA by aflatoxin B1 during hepatocarcinogenesis.
Administration of the hepatic carcinogen aflatoxin B1 to experimental animals results in covalent binding to liver mitochondrial DNA at concentrations three to four times higher than nuclear DNA. The concentration of carcinogen adducts in mitochondrial DNA remains unchanged even after 24 hours, possible because of lack of excision repair. Similarly, mitochondrial transcription and translation remain inhibited up to 24 hours suggesting long-term effects of aflatoxin B1 on the mitochondrial genetic system.
D016604:Aflatoxin B1; D000348:Aflatoxins / Q000378:metabolism*; D000818:Animals; D004272:DNA, Mitochondrial / Q000378:metabolism*; D007700:Kinetics; D008113:Liver Neoplasms / Q000139:chemically induced* / Q000378:metabolism; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism*; D009374:Neoplasms, Experimental / Q000139:chemically induced; D014176:Protein Biosynthesis / Q000187:drug effects; D051381:Rats; D014158:Transcription, Genetic / Q000187:drug effects
D000348:Aflatoxins; D004272:DNA, Mitochondrial; D016604:Aflatoxin B1